Sodium sensitivity and cardiovascular events in patients with essential hypertension

Morimoto, Akira; Uzu, Takashi; Fujii, Takashi; Nishimura, Masataka; Kuroda, Setsuko; Nakamura, Satoko; Inenaga, Takashi; Kimura, Genjiro

doi:10.1016/s0140-6736(97)05189-1

Cited by 422 publications

(298 citation statements)

References 29 publications

Supporting

Mentioning

277

Contrasting

Unclassified

Order By: Relevance

“…Salt‐sensitive hypertensive individuals display a higher rate of cardiovascular events than salt‐resistant hypertensive individuals 1. A similar trend characterizes salt‐sensitive normotensives, who also have a significant increase in mortality rate over time 2.…”

Section: Introductionmentioning

confidence: 78%

Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals

Castiglioni

Parati

Lazzeroni

et al. 2016

JAHA

View full text Add to dashboard Cite

BackgroundEven if sodium sensitivity represents a risk factor at any blood pressure (BP) level, limited evidence is available that it may influence cardiovascular control in normotensives, particularly in white individuals. Therefore, the aim of the study was to investigate whether sodium sensitivity alters hemodynamic or autonomic responses to salt in normotensives.Methods and ResultsWe evaluated the Sodium‐Sensitivity Index (SS‐Index) in 71 white normotensives after 5 days of high‐ and low‐sodium diets. We measured BP continuously at the end of each period, estimating hemodynamic indices from BP waveform analysis, and autonomic indices from heart rate (HR) and BP variability. According to the SS‐Index distribution, we defined 1 sodium‐sensitive group (SS, with SS‐Index >15 mm Hg/[mmol·day]), 1 sodium‐resistant group, (unresponsive to sodium load with −15≤ SS‐Index ≤+15), and 1 inverse sodium‐sensitive group, responsive to sodium by decreasing BP, with SS‐Index <−15). We compared the effects of the diets among groups, and correlated autonomic/hemodynamic indices with the SS‐Index. After sodium loading, a significant decrease in systemic peripheral resistances, HR, spectral indices of BP modulation, and a significant increase of indices of HR vagal modulation were found in the inverse sodium‐sensitive group but not in SS normotensives. Moreover, the highest SS‐Indices were associated with the lesser vagal HR decelerations.ConclusionsOur data suggest that salt sensitivity in white normotensive individuals is associated with impaired vasodilation and altered autonomic response to dietary salt. Such dysfunction may critically contribute to induce a BP response to dietary salt.

show abstract

Section: Introductionmentioning

confidence: 78%

Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals

Castiglioni

Parati

Lazzeroni

et al. 2016

JAHA

View full text Add to dashboard Cite

show abstract

“…[1][2][3][4][5] Although the pathogenesis of salt sensitivity is unknown, both genetic and environmental factors appear to interact to determine the exaggerated BP response to changes in salt intake. [6][7][8][9][10][11][12][13][14][15] Increased reactivity of BP to salt is commonly observed in subjects with obesity and associated cardiovascular risk factors.…”

Section: Introductionmentioning

confidence: 99%

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

2007

View full text Add to dashboard Cite

Salt sensitivity is associated with obesity, and increased cardiovascular morbidity and mortality. We investigated whether treatment of obesity and its associated metabolic abnormalities corrects salt sensitivity and restores impaired nitric oxide (NO) metabolism characteristic of salt sensitivity. Twenty, otherwise, healthy obese saltsensitive subjects completed a 12-month program of caloric restriction, aerobic exercise and metformin. Two salt sensitivity tests were performed, that is at baseline and end of program. Lifestyle-metformin treatment decreased weight (9.870.3 kg), body mass index (3.970.2 kg/m 2 ), waist (11.570.5 cm), systolic blood pressure (SBP) (8.670.4 mm Hg), diastolic blood pressure (DBP) (5.570.4 mm Hg), triglyceride (4075 mg/dl), fasting (8.371 lIU/ml) and post-load (2074 lIU/ml) insulin levels, and salt sensitivity. Going from a highsodium (B300 mmol) to a low-sodium diet (B30 mmol of sodium/day) lowered SBP/DBP by 14.771.7/7.470.9 mm Hg at baseline and by 8.671.9/3.271.2 mm Hg after treatment (Po0.001). More importantly, blood pressure (BP) sensitivity to customary levels of dietary salt (B150 mmol of sodium/day) was abolished by the lifestyle-metformin treatment. Differences in SBP/DBP between usual and low salt averaged 1171/871 mm Hg before treatment, and 371/170.5 mm Hg after treatment (Po0.001). At baseline, NO-metabolite excretion was inhibited during high salt; this impairment was corrected by the lifestyle-metformin treatment. In conclusion, acquired correctable factors play an important role in the pathogenesis of salt sensitivity associated with obesity. Correction of salt sensitivity may account for the BP lowering induced by weight reduction. Restoration of the inability to increase or sustain NO production in response to high salt could account for the correction of salt sensitivity induced by the lifestylemetformin treatment.

show abstract

“…A large proportion of individuals with essential hypertension are salt-sensitive (Kawasaki et al, 1978;Fujita et al, 1980;Weinberger, 1996) and this salt sensitivity is considered to be a marker of the potential for cardiovascular disease (Morimoto et al, 1997;Raij, 1999). A high salt intake has been recognized to be closely correlated with blood pressure elevation (Dahl et al, 1967;Tobian, 1991).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of vascular soluble guanylate cyclase induced by high salt intake in spontaneously hypertensive rats

Kagota

Tamashiro

Yamaguchi

et al. 2001

British J Pharmacology

View full text Add to dashboard Cite

1 Cyclic guanosine monophosphate (cyclic GMP)-mediated mechanism plays an important role in vasodilatation and blood pressure regulation. We investigated the e ects of high salt intake on the nitric oxide (NO) ± cyclic GMP signal transduction pathway regulating relaxation in aortas of spontaneously hypertensive rats (SHR). 2 Four-week-old SHR and normotensive Wistar-Kyoto rats (WKY) received a normal salt diet (0.3% NaCl) or a high salt diet (8% NaCl) for 4 weeks. 3 In aortic rings from SHR, endothelium-dependent relaxations in response to acetylcholine (ACh), adenosine diphosphate (ADP) and calcium ionophore A23187 were signi®cantly impaired by the high salt intake. The endothelium-independent relaxations in response to sodium nitroprusside (SNP) and nitroglycerin were also impaired, but that to 8-bromo-cyclic GMP remained unchanged. On the other hand, high salt diet had no signi®cant e ects on the relaxations of aortic rings from WKY. 4 In aortas from SHR, the release of NO stimulated by ACh was signi®cantly enhanced, whereas the production of cyclic GMP induced by either ACh or SNP was decreased by the high salt intake. 5 Western blot analysis showed that the protein level of endothelial NO synthase (eNOS) was slightly increased, whereas that of soluble guanylate cyclase (sGC) was dramatically reduced by the high salt intake. 6 These results indicate that in SHR, excessive dietary salt can result in downregulation of sGC followed by decreased cyclic GMP production, which leads to impairment of vascular relaxation in responses to NO. It is notable that chronic high salt intake impairs the sGC/cyclic GMP pathway but not the eNOS/NO pathway.

show abstract

Sodium sensitivity and cardiovascular events in patients with essential hypertension

Cited by 422 publications

References 29 publications

Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals

Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

Downregulation of vascular soluble guanylate cyclase induced by high salt intake in spontaneously hypertensive rats

Contact Info

Product

Resources

About